ABSTRACT
Calcium-containing biochar ï¼ES-BCï¼ was prepared by pyrolyzing eggshell and kitchen wastesï¼ and the ES-BC composite was used to remove phosphate ï¼marked as ES-BC/Pï¼. Based on the high affinity of phosphate and carbonate to leadï¼ the ES-BC/P was then used to remove lead from the water. The results showed thatï¼ in the appropriate dosageï¼ ES-BC/P could remove lead efficiently at different initial concentrations ï¼1-100 mg·L-1ï¼ï¼ and the removal efficiency could reach to 99%. Meanwhileï¼ the release of phosphorus could be ignored after the reaction. As ES-BC/P was alkalineï¼ and the lead-containing solution was weakly acidicï¼ the addition of ES-BC/P could adjust the pH of the system automatically. The reaction kinetics and isotherm experiments showed that the lead removal by ES-BC/P was mainly monolayer chemisorption with a maximum adsorption capacity of 493.12 mg·g-1 ï¼318 Kï¼. The characterization results showed that lead was mainly removed through the ion exchanges of Pb2+ in the solution with Ca2+ in ES-BC/P. Thenï¼ the Pb2+ combined with CO32- and PO42- to form many precipitatesï¼ including Pb5ï¼PO4ï¼3OHï¼ Pb10ï¼PO4ï¼6ï¼OHï¼2ï¼ PbCO3ï¼ and Pb3ï¼CO3ï¼2ï¼OHï¼2. In summaryï¼ the ES-BC/P material could achieve the efficient removal of lead from the waterï¼ thereby realizing the resource utilization of the wastes.
ABSTRACT
There is a significant need for additional therapy to improve outcomes for newborns with acute Hypoxic-ischemic (HI) encephalopathy (HIE). New evidence suggests that insulin could be neuroprotective. This study aimed to investigate whether intranasal insulin attenuates HI-induced brain damage and neurobehavioral dysfunction in neonatal rats. Postnatal day 10 (P10), Sprague-Dawley rat pups were randomly divided into Sham + Vehicle, Sham + Insulin, HI + Vehicle, and HI + Insulin groups with equal male-to-female ratios. Pups either had HI by permanent ligation of the right common carotid artery followed by 90 min of hypoxia (8% O2) or sham surgery followed by room air exposure. Immediately after HI or Sham, pups were given fluorescence-tagged insulin (Alex-546-insulin)/vehicle, human insulin (25 µg), or vehicle in each nare under anesthesia. Shortly after administration, widespread Alex-546-insulin-binding cells were detected in the brain, primarily co-localized with neuronal nuclei-positive neurons on double-immunostaining. In the hippocampus, phospho-Akt was activated in a subset of Alex-546-insulin double-labeled cells, suggesting activation of the Akt/PI3K pathway in these neurons. Intranasal insulin (InInsulin) reduced HI-induced sensorimotor behavioral disturbances at P11. InInsulin prevented HI-induced increased Fluoro-Jade C+ degenerated neurons, cleaved caspase 3+ neurons, and volume loss in the ipsilateral brain at P11. There was no sex-specific response to HI or insulin. The findings confirm that intranasal insulin provides neuroprotection against HI brain injury in P10 rats associated with activation of intracellular cell survival signaling. If further pre-clinical research shows long-term benefits, intranasal insulin has the potential to be a promising non-invasive therapy to improve outcomes for newborns with HIE.